Over 200 million people were infected during the coronavirus disease 2019 (COVID-19) pandemic, and over 4.5 million of those cases resulted in death. While the majority of survivors made a full recovery, others developed what are now known as long-haul symptoms, or Long COVID.

Background

Heart damage appears to be a significant long-term clinical effect of COVID-19. This has been known since the outbreak in Wuhan, China. The condition at that time was causing high levels of cardiac troponin, a molecular indicator of myocardial injury, in a number of hospitalized individuals.

These patients’ echocardiographic evaluations revealed that their hearts had functional abnormalities. It was evident that there was a correlation between the severity of COVID-19 and the existence of cardiac damage.

“It was quite clear that people that came into the hospital sick that had heart injury were the ones that were at greatest risk of requiring mechanical ventilation and, ultimately, at the greatest risk of dying.” ____Aaron Baggish, of Massachusetts General Hospital

However, the question of how common this consequence is still unsolved because to the high number of asymptomatic instances and a lack of dedicated research. Furthermore, it’s unclear if myocarditis or the COVID-19’s systemic inflammatory response is to blame for the damage to the heart muscle.

Most significantly, given the enormous number of infections that have happened thus far, the likelihood of long-term harm is still unknown at this time, despite the fact that it is highly significant.

Myocarditis

At least in some patients, heart inflammation seems to be a common feature of COVID-19. This could cause extreme weariness in the absence of other clear signs, affecting both the myocardium and the pericarditis.

In COVID-19, myocarditis is frequently fulminant and usually resolves on its own, while it can also infrequently cause arrhythmias, heart failure, cardiac arrest, and unexpected death. In this instance, cardiogenic shock is the cause of death.

The absence of diagnostics and diagnostic protocols contributes to the largely erroneous diagnosis of myocarditis. Because of this, the exact nature of the sickness is unknown at this time; nevertheless, preliminary reports have indicated that symptoms persisted for a median of 47 days prior to cardiac magnetic resonance imaging (CMR) diagnosis.

In one investigation, edema in more than half the patients indicated ongoing inflammation; many also showed decreased right ventricular function and scarring.

Nevertheless, after two to three months, up to 60% of patients in a different German study which only included those who had successfully gotten rid of the virus as determined by a negative nasal swab remained to exhibit symptoms of cardiac inflammation. More still had elevated troponin levels. In contrast to controls, heart hypertrophy and ineffective pumping were found in this investigation.

In a small number of individuals with significant CMR alterations, active inflammation was verified by cardiac muscle biopsy. The majority of the non-hospitalized patients in this study had a mean age of less than 50 years, and several of them were asymptomatic. The likelihood of cardiac inflammation was unrelated to the severity of COVID-19, underlying medical disorders, or the amount of time from beginning.

In one study, athletes who had recovered from mild or asymptomatic COVID-19 had the same symptoms of myocarditis, whether they were recovering or not. After up to 53 days in quarantine, 12 out of 26 competitive athletes in this study displayed these characteristics.

“The results suggested that scores of otherwise healthy people who recovered from COVID-19—even those who didn’t get very sick—could have potentially harmful inflammation smoldering in their hearts months later.”

Interestingly, a large number of patients in the German study reported symptoms that could have been associated with myocarditis, which could have influenced the results of the study. When compared to controls who were matched for the same risk factors, many of the patients with aberrant imaging findings had results that were borderline positive.

The data is insufficient to make a valid comparison between COVID-19 and this data, or to definitively state that the abnormalities are a specific sequel of COVID-19, because other viral respiratory infections are not studied using CMR or troponin.

In cases of viral infection, myocarditis often results from a direct infection of the heart muscle; however, in the case of COVID-19, the cause may also include cytokines that are circulating as a component of systemic inflammation. The latter may account for the arrhythmias and even cardiac ischemia episodes that arise from plaque rupture and fragmentation of the plaque obstructing the heart arteries.

This process is supported by animal models, which demonstrate heart scarring in infected and recovered monkeys but not in controls.

 ACE2 downregulation and myocardial edema

On the other hand, the ubiquitously distributed angiotensin-converting enzyme 2 (ACE2) functions as the viral receptor and has important cardiovascular properties like regular vascular permeability. Therefore, the increased fluid inflow into the heart muscle brought on by COVID-19’s decreased ACE2 expression leads to moderate edema.

This may be made worse by systemic inflammation, which is another COVID-19 characteristic. This cardiac edema may play a significant role in the cardiac damage associated with COVID-19 and can induce extreme, chronic fatigue. It is possible that glucocorticoids, which quickly reduce inflammatory swelling, constitute the mechanism by which these medications lower mortality in patients with severe COVID-19 who are receiving respiratory support.

In addition, blood clots, sepsis, stress-induced cardiomyopathy, and multisystem inflammatory syndrome can be brought on by COVID-19. The troponin levels indicate that severe COVID-19 may exacerbate pre-existing cardiovascular disease.

Cardiac damage and long COVID

Following COVID-19, signs and symptoms of potential heart damage may include extreme exhaustion, palpitations, chest pain, dyspnea, postural orthostatic tachycardia syndrome (POTS) brought on by neurological abnormalities, and elevated troponin levels with an abnormal electrocardiogram, which may be indicative of a heart attack.

Certain cardiologists link these symptoms to damage to the heart. HospitalizedCOVID-19 patients with elevated troponin levels persisted in exhibiting myocardial scarring even in the absence of edema, suggesting that the virus’s harm is irreversible and putting them at danger for heart failure.

The requirement to pump blood through inflamed lungs puts strain on the right side of the heart. This condition is frequently exacerbated by clot formation in the heart and lung blood arteries, which works in tandem with the inflammation to lower the oxygenation of these essential organs. Because mechanical breathing stresses the right ventricle, using a higher positive end-expiratory pressure may make this worse.

COVID-19 in pre-existing heart failure
The prognosis is bad for those who already have heart failure since co-occurring COVID-19 can cause myocardial damage, which can lead to sudden heart failure. The cytokine storm, which includes high levels of interleukins (IL) such as IL3, IL6, IL7, and other inflammatory mediators, is likely the cause of heart failure in cases of severe COVID-19.

The elevated amounts of cytokines may result in stress cardiomyopathy and cardiac dysfunction. Even in patients who were previously stable, this results in an abrupt decompensation of the pre-existing heart failure.

ACE inhibitors are linked to positive outcomes during COVID-19; however, their role should be assessed to prevent negative consequences when lung involvement occurs, such as pneumonia and acute respiratory distress syndrome (ARDS). Similarly, medications like azithromycin and hydroxychloroquine that might cause arrhythmias when combined with other risk factors and electrolyte imbalances need to be properly watched, particularly if the patient has coronary artery disease or structural heart disease.

Clinical outcomes

However, more investigation is required to link the imaging results with occurrences that are clinically significant. The consequences need to be considered since myocarditis strains the heart, accounting for more than 10% of young adult sudden cardiac fatalities and known to be potentially lethal in athletes who compete.

Athletes who have mild or asymptomatic COVID-19 may resume intense exercise too soon, putting them at risk for myocarditis-related mortality. Before starting to train again, athletes with moderate-to-severe infections should get cardiac imaging and other testing done, according to the American College of Cardiology (ACC). This precaution has revealed several cases that were previously undiagnosed.

All things considered, though, the clinical implications might not be unsettling. According to some scientists, intense athletic training may have caused part of the cardiac damage shown in previous trials instead of the viral infection.

Heart attacks, endothelial damage, and myocardial cell death with scarring could result from myocarditis. Patients may appear with heart failure and arrhythmias five to twenty years after permanent fibrosis sets in.